Autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR) are thought to be carried out by adjustments of arteriolar resistance. Two sensing mechanisms are thought to be responsible, a flow sensor in the macula densa that triggers tubulo gomerular feedback, and a pressure sensor in vascular smooth muscle that is responsible for the myogenic response. The distribution of the regulatory load between the two sensors, and the two different frequency responses will be studied with two techniques. The resistance in pre afferent arteriolar arteries will be measured during the transient response to a sudden change in renal artery pressure and compared to total renal vascular resistance, and the pressure-flow characteristics of the renal circulation will be studied with white noise analysis. In experimental nephrotoxic serum nephritis (NSN), loops of Henle will be perfused in situ to test the hypothesis that tubulo glomerular feedback modulates glomerular filtration coefficient-surface area product (KF). The interactions of the renin-angiotensin and prostaglandin systems will be studied to test the hypothesis that these transmitters have enhanced role in GFR regulation in NSN. The mechanism of pressure diuresis and its relation to GFR autoregulation will be investigated using a digital image processing technique to measure tubular flow rate from video images. Regulation of blood flow will be studied in the renal medulla using a computer based method for measuring erythrocyte velocity in individual vasa recta. The sensitivity of their circulation to various agents will be compared with that of the whole kidney. These agents include intrarenal hormones, neurotransmitters such as acetyl choline and catecholamines, and antidiuretic hormone.